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Elastic strain is an effective and thus widely used parameter to control and modify the electrical, optical, and magnetic properties of crystalline solid-state materials. It has a large impact on device performance and enables adjusting the materials functionality. Here, we promote a micromechanical strain enhancement technology to achieve ultra-high strain in semiconductors. The here presented suspended membranes enable the accurate control of the strain on a wafer-scale by standard top-down fabrication methods making it attractive for both device applications and also, thanks to the simplicity of the method, for fundamental research. This review aims at discussing the process of strain enhancement and its usage as an investigation platform for strain-related physical properties. Furthermore, we present design rules and a detailed analysis of fracture effects limiting the strain enhancement.

A lumping of a Markov chain is a coordinatewise projection of the chain. We characterise the entropy rate preservation of a lumping of an aperiodic and irreducible Markov chain on a finite state space by the random growth rate of the cardinality of the realisable preimage of a finite-length trajectory of the lumped chain and by the information needed to reconstruct original trajectories from their lumped images. Both are purely combinatorial criteria, depending only on the transition graph of the Markov chain and the lumping function. A lumping is strongly k-lumpable, if and only if the lumped process is a kth-order Markov chain for each starting distribution of the original Markov chain. We characterise strong k-lumpability via tightness of stationary entropic bounds. In the sparse setting, we give sufficient conditions on the lumping to both preserve the entropy rate and be strongly k-lumpable.

Summary

Introduction

The Anti-Counterfeiting Trade Agreement (ACTA) is a plurilateral agreement aimed at combating the proliferation of counterfeiting within the global economy. It reflects the current tendency towards enhancing the enforcement mechanisms of intellectual property rights at international level. The agreement has caused significant opposition among the general public and within certain institutions of the European Union, in particular the European Parliament, which rejected ACTA with an overwhelming majority on 4 July 2012. Impediments to its adoption have also started to emerge in other countries that participated in the negotiations, including, for example, Switzerland, which postponed its signature, and Australia, which has suspended its ratification process.

There are several reasons for this (most probable) failure, including its negotiation process, which took place outside any of the specialised multilateral fora such as the World Intellectual Property Organization (WIPO) or the World Trade Organization (WTO), and the secrecy that surrounded the agreement, which caused considerable concern and gave rise to widespread speculation on its content and objectives, leading to the development of considerable mistrust. Anyhow, the main reason that made the European Parliament reject the treaty was the lack of clarity of its provisions on “individual criminalization, the definition of ‘commercial scale’, the role of internet service providers and the possible interruption of the transit of generic medicines.”

Summary

Introduction

The Anti-Counterfeiting Trade Agreement (ACTA) is a plurilateral agreement aimed, according to its Preamble, at providing effective and appropriate means for the enforcement of intellectual property rights. The issue is obviously important, since the attractiveness of intellectual property rights risks being seriously undermined if they cannot be enforced in an appropriate manner. For this reason, the creation of an effective system to secure a proper enforcement of intellectual property rights and to combat counterfeiting has been a constant preoccupation of the European Union (EU) over the last few years. Serious efforts have been made and numerous initiatives undertaken by the EU and its member states to improve the European legal framework in this regard. Following an evaluation report published on 22 December 2010, the European Commission has announced its intention to revise the reference text on the topic, the Directive of 29 April 2004, which has now been implemented in all the member states. Work has also started on an amendment of the regulation of 22 July 2003 concerning customs action against goods suspected of infringing certain intellectual property rights. In 2009, the Commission also set up a European Observatory on Counterfeiting and Piracy, one of whose principal objectives is to collect and transmit data on the economic and social consequences of counterfeiting, and whose powers were recently considerably increased. It is only in the sensitive field of criminal penalties for counterfeiting that harmonisation has not yet succeeded, mostly because of the considerable opposition that a proposed directive on this matter encountered within the European Parliament. This resistance ultimately led to the text being withdrawn by the European Commission on 18 September 2010.

The natural course of cognitive performance, electrophysiological alterations and brain atrophy in ageing and Alzheimer's disease (AD) has been investigated in numerous studies, but only few attempts have been made to examine the relationship between clinical, electroencephalographic (EEG) and morphological changes with quantitative methods prospectively over longer periods of time.

Method

Fifty-five patients with clinically diagnosed AD and 66 healthy elderly controls were examined biannually using a cognitive test (CAMCOG), EEG band power and volumetric estimates of brain atrophy.

Results

On average cognitive performance deteriorated by 28 points on the CAMCOG in the AD group, the alpha/theta ratio decreased by 0.2, and the proportion of intracranial cerebrospinal fluid volume increased by 3.5% during a 2-year period. Similar changes were observed after a second 2-year interval. A multiple regression model demonstrated a significant influence of age on cognition and atrophy and a significant influence of the estimated duration of symptoms on cognition, alpha/theta ratio and brain atrophy at the initial examination. Cognitive performance at the first examination exerted significant effects on the performance and also on brain atrophy at re-examination after 2 or 4 years, whereas the EEG and neuroimaging findings at the previous examination were exclusively related to the corresponding findings at the follow-up examinations. In the control group no significant cognitive, EEG and morphological changes were observed after 2 and 4 years.

Conclusion

After 2 consecutive follow-up periods, we were able to verify significant deteriorations of cognition accompanied by neurophysiological and neuroradiological changes in AD, but not in normal ageing. In clinically diagnosed AD, cognitive performance at the follow-up examination could not be predicted by the previous alpha/theta ratio or by the previous degree of global brain atrophy, whereas the cognitive test score determined not only performance, but also structural findings at follow-up. Performance on cognitive tests appears to be a more sensitive indicator of the degenerative process than EEG band-power and morphological changes in manifest AD. Neuroimaging, neurophysiology and genetic risk markers may be more important for the early differential diagnosis than for the prediction of the course of illness.

We examined the differences in volume of the ventricular and extracerebral cerebrospinal fluid spaces in normal ageing and in probable Alzheimer's disease (AD) and we tried to investigate the effects of the severity of illness on the morphometric differentiation of AD and ageing, the principal components underlying brain atrophy in both conditions, and the correlations of these measurements with clinical findings.

The lateral and third ventricles and the anterior and lateral fissures were significantly larger in AD than in normal ageing. The volumes of the lateral ventricle and lateral fissure permitted a highly efficient differentiation between normal ageing and AD even at the mild stage of dementia, and this differentiation was improved further in the more severe stages of illness. We identified one principal component underlying brain atrophy in normal ageing and two components in AD: a ‘grey matter’ component accounting for sulcal and third ventricular enlargement, and a ‘white matter’ component for lateral ventricular enlargement. In AD, most of the volumetric measurements were significantly correlated with cognitive impairment, but in the group of non-demented elderly controls they were correlated with age.

Conclusion

Volumetric indices of brain atrophy permit a highly efficient differentiation between normal ageing and AD even in the mild stages of illness and this demonstrates that substantial structural brain changes have developed in the preclinical phase of illness. We suggest that there is an uncoupling between lateral ventricular enlargement and cortical brain atrophy in AD.

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